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作 者:余小骊[1] 刘莉琼 吴豫[1] 欧阳晓春[1] 王水华[1] 熊文娟[1] 张萃萍[1] 景少巍[1]
机构地区:[1]中国人民解放军第94医院,南昌330002 [2]宜春市人民医院,宜春336000
出 处:《中国免疫学杂志》2014年第1期121-122,125,共3页Chinese Journal of Immunology
基 金:南京军区医药卫生课题资助项目(No.11MB015)
摘 要:目的:检测一氧化碳中毒后迟发性脑病(DEACMP)患者血清中IL-4、IL-10、IFN-γ、TGF-β1的水平,探讨DEACMP与神经免疫的相关性。方法:实验分为一氧化碳中毒后迟发性脑病组(DEACMP组)、急性一氧化碳中毒未发生迟发性脑病组(ACOP组)及健康对照组。应用酶联免疫吸附法(ELISA)测定30例DEACMP患者、27例ACOP患者及28例健康对照者中血清IL-4、IL-10、IFN-γ、TGF-β1水平,运用相关统计方法分析比较各组数值的差异。结果:DEACMP组IL-4水平低于健康对照组(P<0.05),ACOP组低于健康对照组(P<0.05);DEACMP组IL-10水平低于ACOP组(P<0.05),ACOP组高于健康对照组(P<0.05);DEACMP组IFN-γ水平高于ACOP组及健康对照组(P<0.05),ACOP组高于健康对照组(P<0.05);DEACMP组TGF-β1水平低于ACOP组及健康对照组(P<0.05),ACOP组高于健康对照组(P<0.05)。结论:一氧化碳中毒后迟发性脑病的发生与神经免疫损伤机制有关。Objective:To detect the levels of the IL-4, IL-10, IFN-γ, TGF-β1 in the serum with the patient' s condition of delayed eneephalopathy after carbon monoxide poisoning(DEACMP). To explore the relationship between DEACMP and neuroimmunological correlation. Methods: Experiments were divided into three groups: delayed encephalopathy after carbon monoxide poisoning group ( DEACMP), acute carbon monoxide poisoning without delayed encephalopathy group (ACOP) and healthy control group. Using methods of enzyme-linked immuno-sorbent assay (ELISA), we determined the serum levels of IL-4 ,IL-10 ,TGF-β1 and IFN-3, from 30 patients with DEACMP, 27 patients with ACOP and 28 with healthy control. Using statistical analysis compared the difference between three groups. Results: The level of IL-4 in DEACMP was lower than the healthy control group ( P 〈 O. 05 ) ; ACOP group was lower than the healthy control group ( P 〈 0.05 ) ; the level of IL-10 in DEACMP was lower than the ACOP group ( P 〈 0.05 ), the ACOP group was higher than the healthy control group ( P 〈 0.05 ) ; IFN-γ level in the blood of DEACMP group was higher than that of ACOP group and healthy control group (P 〈 0. 05 ) ; ACOP group was higher than the healthy control group (P 〈 0. 05 ) ; TGF-β1 in DEAC- MP group blood level was below the ACOP group and healthy control group ( P 〈 0.05 ) ; ACOP group was higher than the healthy control group (P 〈 0.05 ) . Conclusion: The occurrence of delayed eneephalopathy after carbon monoxide poisoning is associated with neural immune mechanism of injury.
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